About this Research Topic
With the successful development of monoclonal antibodies treating Alzheimer’s disease (AD), many opportunities and challenges have risen at the same time. The recent case report associated with anti-amyloid-β drug has shown that this drug, Lecanemab, is linked to death in an AD patient with stroke given tissue plasminogen activator (tPA). The negative outcome of the recent phase 3 clinical trial suggests that there is a significant risk of cerebral hemorrhage, particularly in the parenchymal blood vessels adjacent to the caudate nucleus but not directly into the periventricular regions, when tPA is administered for acute ischemic stroke. Including this issue on stroke and AD, the recent advancement is that monoclonal antibodies may pose a risk of adversely interacting with comorbid conditions or drugs designed to treat a single disease.
Review articles, clinical or research insights (suggesting a novel hypothesis), and research articles are sought to provide a clearer scientific picture to reduce the complexities of the decision making regarding the next steps for health care professionals and the translational research community. This Research Topic aims to summarize what we do not know but should know regarding the ‘co-use of a second drug with anti-amyloid-beta approach’ in stroke and AD alike.
In this Research Topic, we look for an answer to the questions:
• Why is a subset of AD patients vulnerable to cerebral hemorrhage when other drugs, such as tPA, is combined with anti-amyloid-β approach (Lecanemab)?
• Other than not using tPA for patients with both stroke and AD, what other translational approach can be an alternative?
• Could changing the sequence of administering each drug avoid the side effect?
• Would there be a drug-specific different response if co-administered with the second drug, given monoclonal antibodies such as lecanemab, aducanubam, and/or donanemab are available, at least, in part?
• What are the current therapeutic approaches mitigating symptoms of AD without risk of developing an adverse effect such as brain hemorrhage?
• What is the current status of monoclonal antibodies such as lecanemab, aducanubam, and/or donanemab, if co-used with other drug(s) such as tPA?
Researchers working in intracranial hemorrhage, subarachnoid hemorrhage, brain hematoma, and post-hemorrhagic hydrocephalus are welcome for their insight, input, and novel approach in treating patients with bleeding in the central nervous system.
Review articles, clinical or research insights (suggesting a novel hypothesis), and research articles are sought to provide a clearer scientific picture to reduce the complexities of the decision making regarding the next steps for health care professionals and the translational research community. This Research Topic aims to summarize what we do not know but should know regarding the ‘co-use of a second drug with anti-amyloid-beta approach’ in stroke and AD alike.
In this Research Topic, we look for an answer to the questions:
• Why is a subset of AD patients vulnerable to cerebral hemorrhage when other drugs, such as tPA, is combined with anti-amyloid-β approach (Lecanemab)?
• Other than not using tPA for patients with both stroke and AD, what other translational approach can be an alternative?
• Could changing the sequence of administering each drug avoid the side effect?
• Would there be a drug-specific different response if co-administered with the second drug, given monoclonal antibodies such as lecanemab, aducanubam, and/or donanemab are available, at least, in part?
• What are the current therapeutic approaches mitigating symptoms of AD without risk of developing an adverse effect such as brain hemorrhage?
• What is the current status of monoclonal antibodies such as lecanemab, aducanubam, and/or donanemab, if co-used with other drug(s) such as tPA?
Researchers working in intracranial hemorrhage, subarachnoid hemorrhage, brain hematoma, and post-hemorrhagic hydrocephalus are welcome for their insight, input, and novel approach in treating patients with bleeding in the central nervous system.
Keywords: tpa, Alzheimer's disease, treatment, tissue plasminogen activator, amyloid-beta
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